Several theories have been proposed to explain the pathophysiology of gait dysfunction in normal pressure hydrocephalus (NPH). The variety of potential targets includes midbrain compression or atrophy, cortical dysfunction, cortical-subcortical or intracortical circuit abnormalities, postural disturbance, dopamine signaling abnormalities, and regional cerebral blood flow (rCBF) depression. This chapter presents objective measures of gait dysfunction that have been used clinically, and highlights some of the major theories postulated to explain gait dysfunction in NPH. Gait dysfunction in NPH has characteristic features that include a slow pace, short stride length, wide stance, and low foot-floor elevation. Objective measures of gait can be used to quantify the pattern of walking and step-taking, focusing on walking speed, stride length, cadence, equilibrium, and posture. Recognition of cortical involvement in locomotion stems from multiple research efforts evaluating gait in healthy individuals and those with cognitive disturbances.